If you were to tour a certain lab at Stanford University, you’d find some very svelte mice. After ingesting a newly discovered compound identified by researchers in a study published this morning in Nature Metabolism, obese mice dropped a considerable amount of weight (relatively speaking, of course). While our metabolisms aren’t dead ringers for mouse metabolisms, the effects of the compound in mice suggest that it could potentially become the next big weight-loss drug for us humans.
Pathology researchers in the Stanford lab, collaborating with postdocs from the Universities of South Florida and Colorado Boulder, had been studying how pythons experience a series of digestion-related changes. Because pythons can eat massive meals and then don’t have to eat again for a few months, they’re metabolically adapted for extreme cycles of feast and famine. In blood samples from young Burmese pythons (Python bivittatus), the researchers detected a metabolite molecule (pTOS) that spiked more than a thousandfold after a meal comprising about 25 percent of their body weight.
“We wondered whether this metabolite affected any of the post-feeding physiological changes in the snake,” explained senior study author Jonathan Long in a press release. “But when we administered pTOS to laboratory mice at levels similar to what we saw in the pythons after eating, we didn’t see any effect on energy expenditure, beta cell proliferation, or organ size.”
Read more: “The Secrets of Deadly Snake Bites”
However, mice that received pTOS lost their appetites and 9 percent of their body weight over the 28-day monitoring period, while maintaining their water intake, energy levels, and movements. The effect mirrors that of GLP-1 medications like Ozempic, but the researchers found that the mechanism was distinct. Semaglutide medications reduce the rate of stomach emptying to sustain the feeling of “full” for longer. Python pTOS doesn’t.
Instead, “pTOS is produced after a meal through the metabolism of tyrosine in the gut and the liver,” explained Long. “It then goes to a region of the brain called the hypothalamus, which is a well-known regulator of energy homeostasis.” Once in the hypothalamus, the python pTOS turns on neurons that regulate feeding behaviors.
In reviewing existing datasets of healthy human volunteers before and after meals, the researchers found that the majority (five of six) showed spikes in pTOS after eating. It typically spiked by only a several-fold (again, compared to a thousandfold in pythons), with one outlier experiencing a 25-fold increase. In fairness, though, since we eat only 1 to 2 percent of our body weight per meal, you’d expect humans to have “a relatively narrow physiologic and metabolic range” compared to pythons, said Long.
“Obviously, we’re not snakes,” he continued. “But maybe by studying these animals we can identify molecules or metabolic pathways that also affect human metabolism.” 
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